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2011 | 71 | 2 |

Tytuł artykułu

Cellular neuropathology of absence epilepsy in the neocortex: a population of glial cells rather than neurons is impaired in genetic rat model

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
It is well accepted that absence epilepsy is not accompanied by structural brain abnormalities. In the present report, we challenged this view based on microscopic analysis of neocortex in a genetic model of absence epilepsy, WAG/Rij rats. Density of neurons and glial cells was measured in the motor, somatosensory and cingular cortical areas in epileptic WAG/Rij rats and in non-epileptic control ACI rats. More extensive and significant differences between two strains were found in a population of glial cells and less significant - in neurons. In contract to ACI rats, WAG/Rij rats showed (1) a deficit of glial cells and a lower glia-neuron index in the somatosensory and cingulate areas (deep layers); (2) a reduced number of neurons locally in the motor cortex. The somatosensory cortex (deep layers) is known to play a key role in triggering of epileptic discharges, and an impairment of glia-neuron interactions in this area might underlie pathological processes in a primary epileptic focus. In the motor cortex, epileptiform activity is known to reach the highest amplitude, and this may cause or result from a deficit of neurons. Our data suggest the critical role of glial cells and glia-neuron interactions in pathogenesis of absence epilepsy.

Słowa kluczowe

Wydawca

-

Rocznik

Tom

71

Numer

2

Opis fizyczny

p.263-268,fig.,ref.

Twórcy

autor
  • Institute of Higher Nervous Activity RAS, Moscow, Russia
autor
  • Institute of Higher Nervous Activity RAS, Moscow, Russia
  • Institute of Higher Nervous Activity RAS, Moscow, Russia
  • Institute of Higher Nervous Activity RAS, Moscow, Russia

Bibliografia

  • Caplan R, Siddarth P, Stahl L, Lanphier E, Vona P, Gurbani S, Koh S, Sankar R, Shields WD (2008) Childhood absence epilepsy: behavioral, cognitive, and linguistic comorbidities. Epilepsia 49: 1838-1846.
  • Coenen AML, van Luijtelaar EL (2003) Genetic animal models for absence epilepsy: a review of the WAG/Rij strain of Rats. Behav Genetics 33: 635-655.
  • D'Antuono M, Inaba Y, Biagini G, D'Argancelo V, Avoli M (2006) Synaptic hyperexcitability of deep layer neocorti- cal cells in a genetic model of absence seizures. Genes Brain Behav 5: 73-84.
  • Depaulis A, van Luijtelaar EL (2005) Genetic models of absence epilepsy in the rat. In: Models of seizures and epilepsy (Pitkänen A, Schwartzkroin PA, and Moshe SL; eds.) Elsevier Academic Press, Amsterdam. pp. 233­248.
  • Fröhlich F, Bazhenov M, Iragui-Madoz V, Sejnowski TJ (2008) Potassium dynamics in the epileptic cortex: new insights on an old topic. Neuroscientist 14: 422-433.
  • Herrup K, Yang Y (2007) Cell cycle regulation in the post- mitotic neuron: oxymoron or new biology. Nat Rev Neurosci 8: 368-378.
  • Inoue M, Peeters BW, van Luijtelaar EL, Vossen JM, Coenen AM (1990) Spontaneous occurrence of spike-wave dis­charges in five inbred strains of rats. Physiol Behav 48: 199-201.
  • Karpova AV, Bikbaev AF, Coenen AM, van Luijtelaar G (2005) Morphometric Golgi study of cortical locations in
  • WAG/Rij rats: the cortical focus theory. Neurosci Res 51: 119-128.
  • Koepp MJ, Duncan JS (2004) Epilepsy. Curr Opin Neurol 17: 467-474.
  • Kulikova SN, Sitnikova EIu, Raevskii VV. (2009) Cytomorphological features of the neocortex in rats with genetic predisposition to absence epilepsy. [in Russian] Zh Vyssh Nerv Deiat Im I P Pavlova. 59: 506-512.
  • Meencke HJ (1989) Pathology of childhood epilepsies. Cleveland Clinic Journal of Medicine 56: S111-S120.
  • Meeren HK, Pijn JP, van Luijtelaar EL, Coenen AM, Lopes da Silva FH (2002) Cortical focus drives widespread corticothalamic networks during spontaneous absence sei­zures in rats. J Neurosci 22: 1480-1495.
  • Midzianovskaia IS, Kuznetsova GD, Coenen AM, Spiridonov AM, van Luijtelaar EL (2001) Electrophysiological and pharmacological characteris­tics of two types of spike-wave discharges in WAG/Rij rats. Brain Res 911: 62-70.
  • Panayiotopoulos CP (1999) Typical absence seizures and their treatment. Arch Dis Child 81: 351-355.
  • Paxinos G, Watson C (1986) The rat brain in stereotaxic coordinates. Academic Press, New York.
  • Paxinos G (2004) The Rat Nervous System. 3rd Edition. Elsevier Academic Press, New York. p: 1328
  • Richardson M (2010) Current themes in neuroimaging of epilepsy: brain networks, dynamic phenomena, and clini­cal relevance. Clin Neurophysiol 121: 1153-1175.
  • Roitbak AI (1999) Glia and its role in nervous activity (in Russian). In: Gliya I ee rol' v deyatelnosti nervnoi sistemi. Izdat. Nauka, S. Petersburg. p. 233.
  • Sarkisova KIu, Kulikov MA, Shatskova AB. (2005) Are WAG/Rij rats with genetic absence epilepsy anxious (in Russian)? In: Zh Vyssh Nerv Deiat Im I P Pavlova. 55: 253-261.
  • Sitnikova E, van Luijtelaar G (2006) Cortical and thalamic coherence during spike-wave seizures in WAG/Rij rats. Epilepsy Res 71: 159-180.
  • Tutkun E, Ayyildiz M, Agar E (2010) Short-duration swim­ming exercise decreases penicillininduced epileptiform ECoG activity in rats. Acta Neurobiol Exp (Wars) 70: 382-389.
  • van Luijtelaar G, Sitnikova E (2006) Global and focal aspects of absence epilepsy: the contribution of genetic model. Neurosci Biobehav Rev 30: 983-1003.

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